Inflammatory signaling is necessary both for innate and adaptive immune responses. Whereas innate immune responses are associated with physiological processes such as wound healing, chronic inflammation culminates inpathological conditions leading to aggravation of inflammatory diseases.Several reports have elegantly demonstrated the involvement of Toll-likereceptors (TLRs), NF-kB and CCAAT/enhancer binding proteins (CEBPs) in the initiation and amplification of the inflammatory response (Litvak et al, 2010; Goldszmid and Trinchieri, 2012), however very little is known about how the inflammatory response is resolved, a process which is crucial for the benefit of the host.